Peripheral nerve injuries constitute a frequent and disabling condition, with an estimated incidence of 23 out of every 100,000 persons per year in developed countries. This statistic does not account for non-traumatic cases (i.e. nerve damage secondary to abdominal or pelvic surgeries) and for lesions not treated at health facilities. Despite great advances in microsurgical techniques, nerve repair continues to be suboptimal, and full functional recovery is seldom achieved. There is thus an imminent need to develop novel strategies to enhance neuroregeneration and optimize return of function.
Research in peripheral nerve injuries has shown that the formation of scar and fibrosis at the site of nerve coaptation impedes axonal regeneration. Furthermore, a negative correlation between the degree of functional recovery and the amount of scar formation at the repair site is a well-established phenomenon. Although nerve regeneration normally occurs at the rate of 1 to 3 mm per day, regenerating axons may require up to 20 to 40 days to traverse the scar at the site of nerve repair. Reduction in scar formation at a site of nerve repair is associated with better recovery. Mechanistically, scarring at the nerve repair site is due to invasion of inflammatory cells, with subsequent upregulation of fibrogenic cytokines.
It would therefore be beneficial to provide an inert barrier around the coaptation site that prevents inflammatory cells infiltration while still allowing diffusion of nutrients and other growth factors to promoting nerve regeneration.